Abstract. GFR and renal plasma flow (RPF) decrease in preeclampsia, a serious hypertensive complication of pregnancy. Serial data derived in late pregnancy (LP) and Ͼ5 mo postpartum (PP) in 13 healthy controls and 10 preeclamptic women (13 and 5, respectively) returning PP for theoretical analysis of neutral dextran sieving curves ( D ), are presented and are used to calculate the key determinants of glomerular ultrafiltration. Normal LP hyperfiltration was associated with increases in RPF and the ultrafiltration coefficient (K f ), as well as in the nondiscriminatory shunt pathway ( 0 ) and the SD of pore size (S). Preeclamptic LP showed the largest 0 and S values, indicating a loss of size-selectivity, accompanying reduced K f and RPF, both of which are implicated in the relative hypofiltration. Despite a 100-fold increase in urinary albumin excretion (UAE), LP preeclamptic D values were reduced for the equivalent neutral dextran (36Å), providing indirect evidence for a loss of glomerular barrier charge-selectivity. All the determinants of GFR and all modeled parameters were comparable across both groups PP, strong evidence that preeclamptic glomerular dysfunction resolves.Preeclampsia, a major cause of maternal and fetal morbidity and mortality, is a multisystem disorder affecting, among others, the hepatic, hematologic, and renal systems. The latter include decreases in renal plasma flow (RPF) and GFR as well as proteinuria that may be in the nephrotic range. Impaired RPF and disordered glomerular barrier integrity could both contribute to hypofiltration (1). One goal of our study was to determine the relative contributions of each in preeclampsia; the other being the quantification of glomerular barrier parameters in relation to proteinuria. Renal hemodynamics were analyzed using clearance of PAH and inulin, while fractional dextran clearances ( D ), combined with mathematical modeling, provided glomerular sieving data, including estimation of the ultrafiltration coefficient (K f ) and glomerular porosity. Preeclamptic and healthy women were studied in late pregnancy (LP) and again 5 mo postpartum (PP). Materials and Methods SubjectsThirteen normotensive, healthy white women with no family history or evidence of renal or cardiovascular disease were studied during LP (36 to 38 wk) and again at least 5 mo PP. Ten untreated preeclamptic primigravidae were also studied in LP, of which 5 returned PP. All met the criteria of the International Society for the Study of Hypertension in Pregnancy (ISSHP) for preeclampsia (de novo hypertension Ͼ140/90 mmHg; proteinuria Ͼ500 mg/24 h) (2). When PP, none were hypertensive, ingesting oral contraceptives, taking medication or breast-feeding. All gave informed written consent to protocols approved by the Joint Ethics Committee of Newcastle and North Tyneside Health Authority and the Universities of Newcastle upon Tyne and Northumbria at Newcastle. ProtocolsOn the study morning, each subject ate a light carbohydrate breakfast but avoided tea and coffee. A 24-h urine collecti...
Studies on intact animals and isolated rat hepatocytes have shown that arginine vasopression (AVP) stimulates glycogen phosphorylase to break down glycogen and raise plasma glucose concentrations. Since no similar work has been performed on healthy human adults, the effect of moderate (25 pmol/min) and high (75 pmol/min) dose AVP infusion on plasma glucose, intermediary metabolites, glucose kinetics, and circulating glucagon and insulin concentrations was investigated. After AVP infusion, plasma glucose rose from 4.9 +/- 0.1 to a peak of 5.7 +/- 0.2 mmol/l (P less than 0.001), but no changes in blood lactate, pyruvate, alanine, glycerol or 3-hydroxybutyrate concentrations were observed. The glucose rise was accounted for entirely by an increase in the rate of appearance of glucose from 11.19 +/- 0.43 to 13.38 +/- 0.63 mu mol/kg/min (P less than 0.001). Infusion of AVP also increased plasma glucagon concentrations from 38 +/- 8 to 79 +/- 20 pg/l (P less than 0.01). The hyperglycaemic effect of AVP may be mediated solely by stimulation of glucagon release, but we cannot exclude direct stimulation of glycogen phosphorylase activity.
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